patient or a caregiver can drain fluid as needed to palliate dyspnea related to the effusion.
Pneumothorax
Air is not normally present between the visceral and parietal pleural surfaces, but it can be introduced into the pleural space by a break in the surface of either pleural membrane, creating a pneumothorax. Because pressure within the pleural space is subatmospheric, air readily enters the space if there is any communication with air at atmospheric pressure.
Etiology and pathogenesis
When a pneumothorax is created by entry of air through the chest wall and parietal pleura, the most common causes are (1) trauma (e.g., knife or gunshot wound) and (2) introduction of air via a needle, catheter, or incision through the chest wall and into the pleural space. Alternatively, air may enter the pleura through a break in the visceral pleura, allowing communication between the airways or alveoli and the pleural space. Examples of the latter circumstance include rupture of a subpleural air pocket (e.g., bleb, cyst, or bulla) into the pleural space or necrosis of the lung adjacent to the pleura by a destructive pneumonia or neoplasm.
A pneumothorax can result from a break in the parietal pleura (e.g., from trauma, needle, or catheter insertion) or in the visceral pleura (e.g., from rupture of a subpleural air pocket or necrosis of lung adjacent to the pleura).
When a reason for the pneumothorax is apparent, such as an underlying abnormality in the lung, the pneumothorax is called a secondary spontaneous pneumothorax. Common causes include lung diseases known to be associated with subpleural air pockets (emphysema or interstitial lung disease with honeycombing and subpleural cysts), or destruction of lung tissue adjacent to the pleural surface (necrotizing pneumonia or neoplasm). In contrast, some patients do not have a defined abnormality of the lung adjacent to the pleura and therefore are said to have a primary spontaneous pneumothorax. Even in this circumstance, patients frequently have small subpleural pockets of air (blebs), especially at the lung apices, that have gone unrecognized clinically and on routine radiographic examination. If a bleb eventually ruptures, air is released from the lung parenchyma into the pleural space, creating a pneumothorax.
Patients who receive positive pressure to the tracheobronchial tree and alveoli (e.g., with mechanical ventilation) are subject to development of a pneumothorax. In this case, positive pressure may lead to rupture of a preexisting subpleural bleb or penetration of air through an alveolar wall into the interstitial space. The air then tracks through the lung parenchyma to the subpleural surface and eventually ruptures into the pleural space. Alternatively, and perhaps more commonly, the air following alveolar rupture tracks retrograde to the mediastinum alongside blood vessels and airways to produce a pneumomediastinum (see Chapter 16). A pneumothorax can result when air subsequently ruptures through the mediastinal pleura into the pleural space.
Pathophysiology
The pathophysiologic consequences of a pneumothorax are variable, ranging from none to the development of acute cardiovascular collapse. The size of the pneumothorax (i.e., amount of air within the pleural space) is an important determinant of the clinical effects. Because the lung is enclosed within a relatively rigid chest wall, accumulation of a substantial amount of pleural air is accompanied by
collapse of the underlying lung parenchyma. In extreme cases, air in the pleural space occupies almost the entire hemithorax, and the lung is totally collapsed and functionless until the pleural air is resorbed or removed.
Air in the pleural space is generally under atmospheric or subatmospheric pressure. In some cases the air may be under positive pressure, creating a tension pneumothorax. This tension within the pleural space develops due to a “one-way valve” mechanism by which air is free to enter the pleural space during inspiration but the site of entry is closed during expiration. When air repeatedly enters the pleural space but does not exit, the intrapleural pressure increases, and the underlying lung collapses further. When pleural pressure is sufficiently high, the mediastinum and trachea may be shifted away from the side of the pneumothorax. In extreme cases, cardiovascular collapse and respiratory failure may result, with a marked fall in cardiac output and blood pressure. These hemodynamic changes are commonly stated to result from inhibition of venous return into the superior and inferior venae cavae as a consequence of positive intrathoracic pressure. However, in animal models, the predominant pathophysiologic mechanism appears to be progressive respiratory failure with severe hypoxemia and ventilatory compromise. Whatever the mechanism, emergent treatment is necessary to release the air under tension and reverse the process. A particularly important risk factor for development of a tension pneumothorax is positive-pressure ventilation with a mechanical ventilator. When a pneumothorax occurs in this situation, the ventilator may continue to introduce air under high pressure through the site of rupture in the visceral pleura.
A tension pneumothorax may be associated with total collapse of the underlying lung, mediastinal shift, and cardiovascular collapse.
For most cases of pneumothorax, after the site of entry into the pleural space is closed, the air is spontaneously resorbed. The reason is that the pressure of gases in the air in a pneumothorax is higher than the combined partial pressure of those gases in surrounding venous or capillary blood. For example, air within the pleural space might have a pressure a few millimeters of mercury below atmospheric pressure, or approximately 755 to 758 mm Hg. In contrast, gas pressures in mixed venous blood are approximately as follows: PO2 = 40 mm Hg, PCO2 = 46 mm Hg, PN2 = 573 mm Hg, and PH2O = 47 mm Hg. Therefore, the total gas pressure in mixed venous blood is 706 mm Hg, which is approximately 50 mm Hg below that of air in the pleural space. Consequently, there is a gradient for diffusion of gas from the pleural space into mixed venous blood. With continued diffusion of gas from the pleural space into the blood, the size of the pneumothorax is slowly reduced, the gas pressures within the pleural space are maintained, and the gradient favoring absorption of gas continues until all the air is resorbed.
If high levels of supplemental O2 are administered to the patient with a pneumothorax, the process of resorption can be hastened. Following application of oxygen, most of the nitrogen in arterial blood is replaced by O2. As a result, PN2 in the capillary blood surrounding the pneumothorax becomes quite low,
and the gradient for resorption of nitrogen from the pleural space time, although arterial PO2 is high after inhalation of pure O2, PO2
is increased considerably. At the same falls substantially in capillary and
venous blood because of O2 consumption by the tissues. Therefore, a large partial pressure gradient from pleural gas to pleural capillary blood remains for O2 as well. The net result is that O2 administration favors more rapid resorption of nitrogen (the main component of gas in ambient air and thus in the pneumothorax) without significantly compromising the gradient promoting resorption of O2.
When a pneumothorax is causing important clinical problems, the physician need not wait for spontaneous resorption of the air but can actively remove the air with a needle, catheter, or tube inserted
into the pleural space.
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Clinical features
In many cases, the patient has obvious risk factors for developing a pneumothorax (e.g., predisposing underlying lung disease, receiving positive-pressure ventilation with a mechanical ventilator). The group of patients in whom a primary spontaneous pneumothorax develops shows a striking predominance of males. In addition, the patients are often smokers, are young adults, and frequently are tall and thin.
Clinical features of pneumothorax: Symptoms: chest pain and dyspnea
Physical signs: asymmetric (decreased) breath sounds, hyperresonance, tracheal deviation (tension), and ↓ blood pressure (tension)
The most common complaint at the time of pneumothorax is acute onset of chest pain, dyspnea, or both, but some patients may be totally symptom-free, particularly if the pneumothorax is small. On physical examination, findings depend to a large extent on the size of the pneumothorax. Because of decreased transmission of sound, breath sounds and tactile fremitus are diminished or absent. With a significant amount of air in the pleural space, increased resonance to percussion over the affected lung may be observed.
When the pneumothorax is under tension, the patient is often in acute distress, and a decrease in blood pressure or even frank cardiovascular collapse may be present. Palpation of the trachea frequently demonstrates deviation away from the side of the pneumothorax.
Diagnostic approach
The diagnosis of pneumothorax most commonly is established or confirmed by chest radiograph, although CT scan and ultrasound have greater sensitivities for small pneumothoraces. The characteristic finding is a curved line representing the edge of the lung (the visceral pleura) separated from the chest wall.
Between the edge of the lung and the chest wall, the pleural space is lucent, and none of the normal vascular markings of the lung are seen in this region (Figs. 15.6 and 15.7). When the pneumothorax is small, separation of the visceral and parietal pleura appears on upright chest films only at the apex of the lung, where the pleural air generally accumulates first. If the pneumothorax is substantial, the lung loses a significant amount of volume and therefore has a greater density than usual.
FIGURE 15.6 Chest radiograph of patient with right-sided spontaneous pneumothorax and underlying COPD. Arrows point to visceral pleural surface of lung. Beyond visceral pleura is air within pleural space. No lung markings can be seen in this region.
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FIGURE 15.7 Chest radiograph of left spontaneous pneumothorax. Arrow points to
edge of the completely collapsed left lung.
When both fluid and air are present in the pleural space (hydropneumothorax), the fluid no longer appears as a meniscus tracking up along the lateral chest wall. Rather, the fluid falls to the most dependent part of the pleural space and appears as a liquid density with a perfectly horizontal upper border, above which is the air in the pleural space (see Fig. 15.8). Finally, when gas in the pleural space is under tension, evidence is often seen of structures (e.g., trachea and mediastinum) being “pushed” away from the side of the pneumothorax (Fig. 15.9).
FIGURE 15.8 Chest radiograph shows right hydropneumothorax. Horizontal line in lower right hemithorax is interface between air and liquid in pleural space. Arrows point to visceral pleura above level of effusion. There is air in pleural space between visceral pleura and chest wall.
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FIGURE 15.9 Chest radiograph shows right-sided tension pneumothorax. No lung
markings are seen in right hemithorax, and mediastinum is shifted to left.
Treatment
Treatment of a pneumothorax is based on the type of pneumothorax as well as by the size and the ensuing clinical consequences. With a primary spontaneous pneumothorax causing few symptoms, it is best to wait for spontaneous resolution. With a large but minimally symptomatic primary spontaneous pneumothorax (involving >20% of the hemithorax), the options are either to evacuate the air with a needle or catheter, or wait for spontaneous resolution. Resolution can be hastened by administration of 100% O2, which alters the partial pressures of gases in capillary blood, favoring resorption of pleural air.
When the pneumothorax is secondary to identifiable underlying lung disease (secondary spontaneous pneumothorax) or the patient has significant clinical sequelae, the air is best removed, usually by a catheter or chest tube inserted into the pleural space. Patients with secondary spontaneous pneumothorax and those with recurrent primary spontaneous pneumothorax often require obliteration of the pleural space by instilling agents, such as talc, into the pleura to promote pleural inflammation and sclerosis. Concomitant thoracoscopic resection of subpleural apical blebs is frequently performed, giving the opportunity to achieve pleurodesis via mechanical irritation of the pleura rather than by agents such as talc.
If a patient has hemodynamic compromise because of a tension pneumothorax, a needle, catheter, or tube must be inserted immediately to relieve the pressure. When this technique is performed, the sound of air under pressure escaping from the pleural space can readily be heard. The most important results of